Homeostasis Feedback Systems

For the body to be in health, it must operate within a very narrow range of acceptable

values for things such as enzyme function, mucus secretion, blood calcium, somatic

reflex arc function, blood glucose, blood oxygen level, heart rate, blood pressure, blood

gas levels, gastric secretions, body temperature, water and ion concentrations, and blood

pH. The body can regulate its internal environment through a multitude of feedback

systems. A feedback system is a cycle of events in which the status of a body condition

is continually monitored, evaluated, changed, remonitored, reevaluated, and so on.

Homeostasis is a condition in which the body‟s internal environment remains within

normal physiological ranges. Homeostasis in the human body is continually being

disturbed. The disruption may come from the external (outside the body) environment in

the form of physical insults such as intense heat or lack of oxygen. Other disruptions

originate in the internal (within the body) environment – for example, a blood glucose

level that is too low. Homeostasis imbalances may also occur due to psychological

stresses in our social environment – the demands of work and school, for example. In

most cases the disruption of homeostasis is mild and temporary, and the responses of

body cells quickly restore balance in the internal environment. In other cases the

disruption of homeostasis may be intense and prolonged, as in poisoning, overexposure to

temperature extremes, severe infection, or death of one‟s spouse. Under these

circumstances, regulation of homeostasis may fail.

Fortunately, the body has many regulating systems that bring the internal environment

back into balance. Most homeostatic responses of the body are regulated by the nervous

and endocrine systems, working separately or together.

The nervous system regulates body activities by sensing deviations from normal

physiological limits and then sending messages in the form of nerve impulses, to organs

to alter the trend of the deviations.

The endocrine system also monitors body functions and sends messages, in the form of

hormones, to regulate homeostasis. Hormonal regulation is achieved more slowly than

nervous regulation of homeostasis.

In the body, achieving homeostasis is often the result of a negative feedback loop. The

stimulus alters the controlled condition. The receptors monitor changes in the controlled

condition resulting from some stimuli. The control center determines the value of the

controlled condition. The response of the effectors is to alter body activities to return the

controlled condition to within normal limits.

A negative feedback system reverses a change in a controlled condition. Negative feedback

systems tend to maintain conditions that require frequent monitoring and adjustment.

Examples would include blood pressure, blood glucose levels, and body temperature. A

positive feedback system tends to strengthen or reinforce a change in one of the body‟s

controlled conditions. Normal childbirth is a good example of a positive feedback system.

Homeostasis of Enzyme Function

Chemical reactions are fundamental to the existence of living cells. These reactions

determine the type and quantity of cellular molecules and are promoted by enzymes,

which are typically protein in structure. As such, each cell‟s appearance and function

depends on the activity of its enzymes.

Each cell may have thousands of enzymes that are responsible for normal metabolic

processes. Among the more important metabolic processes is the ability to convert

different types of fuel molecules, found in food, into energy and thereby fuel cellular

processes. The molecule most used by cells for this purpose is glucose, a

monosaccharide.

Other types of simple carbohydrates that are present in food and converted to glucose are

galactose found in milk, and fructose, found in fruit. Many metabolic processes,

including these conversion reactions, occur with normal functioning of liver enzymes.

We will use the conversion of galactose to glucose to explain enzyme-mediated

metabolic reactions.

If galactose is not converted to glucose, then an adequate amount of glucose may not be

available to power cellular functions. Excessive accumulation of galactose in body

tissues, a disorder called galactosemia, will cause further health problems.

Galactosemia is an inherited metabolic disorder associated with abnormal liver enzyme

function. Enzyme structure is determined by the cell‟s genetic code. Alterations of the

genetic sequence of nucleotides (a gene) may result in inadequate amounts of functioning

enzymes.

In the case of galactosemia, the enzyme needed to convert galactose to glucose is

defective, resulting in an accumulation of galactose in the body. The homeostatic

response that would result from inadequate enzyme function is excessive galactose.

The enzyme reaction that converts galactose to glucose represents only one of nearly

5000 enzyme-mediated metabolic reactions found in liver cells. Understanding the

underlying causes of galactosemia emphasizes the fundamental and vital roles that

enzymes play in regulating homeostasis.

Homeostasis of Mucus Secretion

Although the stimulus for the production of mucus, a normal secretory cell function, is

unknown, mucus plays several positive roles in maintaining good health. In particular,

mucus acts as a lubricant for the linings of the digestive and respiratory tracts.

Glandular epithelial cells form the secretory portions of glands. The secretion of mucus

by exocrine glands is made possible by transporter proteins, which are coded by

sequences of DNA (genes) and assembled by ribosomes and the golgi complex.

By means of transporter proteins, frequently called “transporters,” ions move across the

plasma membrane of a cell into the extracellular fluid. Once the ions, and other solutes,

are moved into the extracellular fluid, their concentration increases the extracellular

fluid‟s osmotic pressure. This decreases the relative concentration of extracellular water.

Water then follows the solutes out of the cell, via osmosis, to form the watery secretion

we call „mucus‟.

Cells synthesize many chemicals to promote homeostasis. These chemicals are produced

or modified by enzymes which, in turn, are created from information in the DNA

templates, or genes. Small changes in the genetic code, and therefore enzymes, may

cause significant homeostatic imbalances.

Cystic Fibrosis (mucoviscidosis) is a recessively inherited disorder (both parents must

contribute its gene to the afflicted offspring) of the exocrine glands, resulting in the

excessive buildup of thick mucus. Because it affects exocrine glands, which are widely

distributed, cystic fibrosis is a multi-organ disease. It is the most common lethal genetic

disease (about 1 in 2000 births), and typically results in death by pulmonary failure.

When the gene that codes for the Cl –

transporters is defective, the resulting defective

transporter protein is not inserted into the plasma membrane of the epithelial cell in the

exocrine gland.

Cystic fibrosis is only one example of the serious effects of mucus imbalance, but it

illustrates the crucial role of proteins in maintaining the balance of fluids and ions

transported across the plasma membrane and thus, normal secretory cell function.

Homeostasis of Blood Ca 2+

The body‟s regulation of blood Ca

2+ levels is crucial to maintaining good health. It‟s

very important to many functions of the body including muscle contraction, neuro-

transmitter release, and blood clotting.

Muscle exertion and pregnancy are two examples of a stimulus that decreases the blood

Ca 2+

levels. (controlled condition)

The receptors in the parathyroid gland cells send message to control center.

The PTH (parathyroid hormone) gene is turned on and the output is increased PTH.

The effectors are:

1. Osteoclasts increase bone resorption.

2. Kidney increases Ca 2+

retention and increased calcitrol production.

The response is increased blood Ca 2+

.

Regulation of blood calcium is very important to many functions of the body, including

muscle contraction, neurotransmitter release, and blood clotting.

Abnormal blood calcium levels may result in a homeostatic disorder.

Osteoporosis is a condition of porous bones characterized by decreased bone mass and

increased susceptibility to fracture. There are several causes of osteoporosis, but one of

the primary causes results from excessive production of PTH (parathyroid hormone),

which regulates blood calcium (Ca 2+)

levels.

One risk factor, female menopause, demonstrates a blood calcium imbalance. In females,

normal levels of estrogen inhibit PTH production. Lowered estrogen levels, which occur

with the onset of menopause, may allow excessive PTH production. Blood calcium

imbalances (both high and low) have a wide range of effects. We have examined only

two of these to help your understanding of the role of Ca 2+

levels in essential

physiological processes such as bone and teeth formation, blood clotting,

neurotransmitter release, maintenance of muscle tone, and excitability of nervous and

muscle tissue. Regulating Ca 2+

levels is a crucial part of maintaining homeostasis.

Energy Sources for Muscle Contraction

1. ATP already in the cell (not much).

2. ATP from cellular respiration – requires oxygen – an aerobic process – too slow

for sustained contraction, but continues.

Occurs in the mitochondria.

1 glucose + oxygen yields 36 ATP + Carbon dioxyide + water.

3. ATP from creatine phosphate – donates PO4 to convert ADP to ATP.

Good for only a few seconds. Phosphate donor from skeletal muscles.

4. ATP from Lactic Acid Fermentation

Anaerobic process that kicks in when insufficient oxygen is in the cell to carry out

the aerobic process.

Instead of 36-38 ATP‟s per glucose, yields only 2 ATP.

Breakdown of muscle glycogen into glucose

and the production of 2 peruvic acid from glucose via glycolysis

yields 2 ATP and lactic acid.

But, fibers also contain myoglobin in red muscle fibers to store oxygen and

glycogen to store glucose.

Problems with Lactic Acid Fermentation:

Lowers pH of cell to the point that enzymes are no longer functional and

contraction stops – muscle fatigue.

Oxygen debt. The amount of oxygen required to recycle all lactic acid in

the cell – 1/5 changed to carbon dioxide and excreted; 4/5 changed to

glycogen and recycled.

Sources of ATP production, in summary:

1. What‟s already there

2. Creatine phosphate

3. Cellular respiration

4. Lactic Acid Fermentation

The Muscle Contraction Cycle

Sarcomeres shorten through repeated cycles during which the myosin heads (cross-

bridges) attach to actin, rotate, and detach.

During the power stroke of contraction, myosin heads rotate and move the thin filaments

past the thick filaments in a wratcheting motion toward the center of the sarcomere.

1. Myosin heads hydrolyze ATP and become reoriented and energized.

2. Myosin heads bind to actin, forming cross-bridges.

3. Myosin heads rotate toward center of sarcomere (power stroke)

4. As myosin heads bind ATP, the cross-bridges detach from actin.

Contraction cycle continues if ATP is available and CA2+

level in the sarcoplasm is high.

Four stages of cross-bridge cycle:

1. Cross-bridge binds to actin.

2. Cross-bridge moves

3. ATP binds to myosin causing cross-bridge to detach.

4. Hydrolysis of ATP energizes cross-bridge.

Why rigor mortis when we die?

Ca 2+

ions leak out of the SR and allow the myosin heads to bind to actin.

But, ATP production has ceased, so the cross-bridges cannot detach from actin.

Therefore, muscles are in a state of rigidity (rigor mortis).

Calcium’s Role in Muscle Contraction

Ca 2+

„s role in the regulation of contraction by troponin and tropomyosin.:

(a) During relaxation, the level of Ca2+

in the sarcoplasm is low because calcium ions

are pumped into the sarcoplasmic reticulum (SR) by Ca2+

active transport pumps.

(b) A muscle action potential propagating along a transverse tubule opens Ca2+

release channels in the SR, calcium ions flood into the cytosol, and contraction

begins.

An increase in the Ca2+

level in the sarcoplasm starts the sliding of thin filaments;

When the level of Ca2+

in the sarcoplasm declines, sliding stops.

Therefore, the sarcoplasmic reticulum (SR) releases Ca 2+

ions to trigger muscle

contraction.

Relaxation:

Troponin holds tropomyocin in position to block myosin-binding sites on actin.

Contraction:

Ca2+

binds to troponin, which changes the shape of the troponin-tropomyosin

complex and uncovers the myosin-binding sites on actin.

Actin binds to active sites when stimulus is switched on.

Physical contact only takes place when sites are uncovered

Sodium / Potassium Pump

Sodium ions are expelled and potassium ions are imported through the sodium pump.

(Na+ / K

+ ATPase).

The pump will not work unless Na+ and ATP are present in the cytosol and K

+ is present

in the extra-cellular fluid.

Na+ in the cytosol binds to the pump protein.

(Na+ concentration is high in the ECF and low in the cytosol, whereas K+ concentration

is high in the cytosol and low in the ECF.)

Na+ binding triggers the breakdown of ATP into ADP and the attachment of a high-

energy phosphate group (P) to the pump protein.

This action changes the shape of the pump protein so that the Na+ is pushed through the

membrane and expelled into the ECF.

The new shape of the pump favors binding of K+ in the ECF.

K+

binding triggers release of the phosphate group from the pump protein, which again

causes the shape of the pump protein to change.

As the pump protein returns to its original shape, K+ is pushed through the membrane

into the cytosol.

At this point, the pump is ready to bind Na+ in the cytosol and the cycle repeats again.

How Information is Carried Along a Neuron in the Body

Information transmission along a neuron in the body involves reversal of polarity,

shifting of Na+ and K

+, action potential, Na

+ permeability and K

+ permeability.

Inter-neurons are triggered by sensory input.

(Motor neurons are not triggered by sensory input; information passes on to interneuron.)

A transmitter substance such as acetylcholine or noradrenalin diffuses to the receptor

sites.

Na+ rushes in to the cell with a change to the permeability of the responding cell.

The neuro-transmitter bonds with the receptor and causes ion channels to open.

Vesicles containing transmitter substance dump the transmitter into the synaptic cleft.

Receptors in the cell membrane of post-synaptic cells receive the transmitter substance.

Na+ rushes in; K+

rushes out of the cell.

The electrical gradient is positive on the outside relative to the inside.

The gated channel opens or closes in response to chemical or electrical changes inside or

outside the cell. When the gate is open, ions can diffuse through the channel.

Depolarization goes in a wave along the neuron. i.e., the message is carried all the way

to the end of the nerve cell. It‟s all or none.

Active transport pumps Na+ back out of the cell.

The impulse is the point at which the polarity is reversed.

What the message means is interpreted at the end of the path.

If the neurons are myelinated, it goes faster because the message jumps from Schwann

cell to Schwann cell by going from a Node of Ranvier to the next Node of Ranvier.

Therefore, the myelinated sheath allows the message to go faster because it doesn‟t have

to repolarize as often.

Activity at Neuro-Muscular Junction

Acetylcholine released at the neuromuscular junction triggers a muscle Action Potential

which leads to muscle contraction.

1. Nerve impulse arrives at axon terminal of motor neu

ron and triggers release of acetylcholine (ACh).

2. ACh diffuses across synaptic cleft, binds to its receptors in the motor end plate,

and triggers a muscle Action Potential (AP).

3. Acetylcholinesterase in synaptic cleft destroys ACh so another muscle Action

Potential does not arise unless more ACh is released from motor neuron.

(ACh agonist = nicotine. ACh antagonist = curare.)

4. Muscle AP travelling along T-tubule opens Ca 2+

release channels in the

sarcoplasmic reticulum (SR) membrane, which allows calcium ions to flood into

the sarcoplasm.

5. Ca 2+

binds to troponin on the thin filament, exposing the binding sites for

myosin.

If a threshold number of receptor sites are filled, then the muscle responds.

6. Contraction: power strokes use ATP;

Myosin heads bind to actin, swivel, and release;

Thin filaments are pulled toward center of sarcomere in wracheting movement.

7. Ca 2+

release channels in SR close and Ca 2+

active transport pumps use ATP to

restore low level of Ca ions in sarcoplasm.

8. Troponin-tropomyosin complex slides back into position where it blocks the

myosin binding sites on actin.

9. Muscle relaxes.

Somatic Reflex Arc Function

The nervous system pathway that rapidly and predictably responds to changes in the

internal and external environment is known as a reflex arc. Autonomic reflex arcs that

control smooth and cardiac muscles as well as endocrine and exocrine glands are very

important to normal body functions.

You are probably most aware of the somatic reflex arcs that control contractions of

skeletal muscles. Somatic reflex arcs provide very rapid adjustments to body

movements.

In most cases, these reflexes also act to prevent injury.

This type of neural pathway, called reciprocal innervation, that contracts one muscle and

relaxes the opposing muscle, allows the reflex to respond very rapidly to abrupt changes

in muscle tension.

Several somatic reflexes can be used to assess neurological damage. Physicians often use

the patellar reflex or knee jerk as one method of evaluating a patient‟s neurological

condition.

In this examination, the physician lightly strikes the patellar ligament with a specialized

rubber-tipped instrument shaped somewhat like a hammer. This action of instrument

against patellar ligament temporarily overstretches the quadriceps muscle group.

Increased motor impulses cause the quadriceps muscles to contract and extend the leg.

The same applied stimulus (hammer strike) causes the hamstring muscles to relax and

allow rapid extension of the leg in a normal knee jerk response.

The patellar reflex is affected when damage occurs to (1) the motor or sensory neurons

that supply the quadriceps, or (2) the lumbar region of the spinal cord. Damage would

cause an absence of control center output to the prime mover muscle.

Unfortunately, if the damage that affects the nerrons of the patellar reflex, or any other

nervous pathway, is permanent then effective treatment may not exist. Studies aimed at

regrowing both nerves and the spinal cord are underway and provide the most hope for

victims of spinal cord injury.

Homeostasis of Blood Glucose

Cells use glucose (sugar) molecules as their primary energy source. Maintaining normal

blood glucose levels is one of the most important regulatory processes in the body. Many

mechanisms, in both the endocrine and nervous systems, can alter blood glucose levels to

bring the body back to homeostasis.

A critical mechanism for regulating blood sugar involves the secretions of the pancreatic

hormones, insulin and glucagon. These hormones operate in an antagonistic manner: to

reach a normal blood sugar level, one hormone acts to lower the blood sugar level while

the other hormone acts to raise it.

Exercising is an example of a stimulus that would result in a decreased blood glucose

level (controlled condition). Receptors in the pancreatic cells send a message to the

control center (glucagon gene in alpha cells). The output is increased glucagon

production which affects the liver. The increased glucagon acts on liver cells to convert

glycogen to glucose, thereby increasing blood glucose levels.

This new stimulus affects the controlled condition (increased blood glucose) which is

detected by the receptors in pancreatic cells. They send a message to the control center

insulin gene in beta cells to cause an increased output of insulin.

The effectors are:

Liver Body Cells Fat Cells

Increased conversion Accelerated uptake of Increased conversion

of blood glucose to glucose and amino acids of blood glucose to

glycogen. into cell and increased fat.

protein synthesis.

The response is decreased blood glucose. The levels of insulin and glucagon change

frequently to provide nearly constant regulation of blood glucose levels.

Both low levels of blood glucose (hypoglycemia) and elevated levels of blood glucose

(hyperglycemia) can have adverse effects on many structures of the body.

Diabetes Mellitus

Diabetes mellitus comprises a group of disorders caused by the inability of cells to

transport glucose into their interior. As a result of this inability, the unused glucose

accumulates in the blood resulting in high blood sugar (hyperglycemia). Without

glucose, the body turns to other fuel sources, such as proteins (amino acids) and lipids

(fatty acids) for cellular metabolism.

These disturbances in carbohydrate, protein, and fat metabolism are characteristic of the

two major forms of diabetes mellitus, type I and type II. Medical researchers believe that

both types of diabetes are caused by interactions between genetic and environmental

factors.

Type I diabetes is caused by a specific homeostatic imbalance. There is a deficient

insulin output which affects the body cells. The response is Type I diabetes mellitus.

Type I diabetes mellitus is also called insulin-dependent diabetes mellitus and is caused

by a deficiency of insulin. Medical researchers believe that it is an autoimmune disease

that attacks the beta cells of genetically predisposed individuals.

Type II diabetes, also called non-insulin-dependent diabetes mellitus, is the most

common form of diabetes. Obesity is the major environmental risk factor that increases

an individual‟s chance of contracting type II diabetes mellitus.

The metabolism of an individual with type I diabetes is similar to that of a starving

person. The primary clinical manifestations of type I diabetes are:

Excessive thirst (polydipsia),

Excessive urination (polyuria), and

Excessive hunger (polyphagia).

Elevated blood glucose causes water to be osmotically transported out of all body cells

including hypothalmic cells. Stimulation of the hypothalamus triggers increased thirst.

This situation causes water to be osmotically transported into the kidney filtrate resulting

in high urine output. Excessive levels of glucose overwhelm the ability of the kidney to

retain glucose in blood thereby causing high levels of glucose in the urine. Cellular

starvation triggers an increase in hunger – inadequate carbohydrate, fat and protein

energy sources.

The most common treatment for insulin-dependent diabetes mellitus (Type I) is the

administration of insulin. The injection of insulin brings the insulin levels in the blood

back to normal thereby promoting a return to homeostasis of blood glucose and,

hopefully, leading to cessation of clinical symptoms.

Homeostasis of Blood Oxygen Levels

The major function of red blood cells (erythrocytes or RBCs) is to transport oxygen

throughout the body. Oxygen chemically binds to hemoglobin molecules and is

transported by the red blood cells. Both the number of red blood cells and the

concentration of hemoglobin within them determine the blood oxygen level.

Cells use oxygen during the process of harvesting energy from fuel molecules, such as

glucose. Not having enough oxygen adversely affects cell metabolism and can result in

cell damage or death.

When the oxygen carrying capacity of the blood drops because red blood cell production

(erythropoiesis) is not adequate, low blood oxygen triggers a negative feedback

mechanism. This mechanism, regulated by the hormone erythropoietin, increases red

blood cell production to bring the body back into homeostasis.

Low blood oxygen is an example of a controlled condition that would promote

production of erythropoietin by kidney cells. The control center red bone marrow causes

an output of increased immature RBCs. The effector is red blood cells – increased RBCs

in circulation. The response is increased blood oxygen. Increased numbers of RBCs will

elevate blood oxygen levels.

If the homeostasis of blood oxygen is disrupted and blood levels are reduced, a condition

called hypoxia occurs.

Anemia is a condition in which the oxygen-carrying capacity of blood is reduced.

Several kinds of anemia exist, all characterized by reduced RBC count, reduced

hemoglobin, or abnormal hemoglobin.

Hemorrhagic, pernicious, and aplastic anemia result from inadequate red blood cell

count.

Hemorrhagic anemia is caused by abnormally low RBC count. The response is decreased

blood oxygen. Hemorrhagic anemia is caused by blood low due to wounds, ulcers, or

heavy menstrual bleeding.

Pernicious anemia is caused by low hemopoiesis, which is caused by the lack of intrinsic

factor, a molecule needed for the absorption of vitamin B12. Adequate vitamin B12 levels

are needed to make red blood cells.

Aplastic anemia can occur following the destruction of red bone marrow from a tumor,

toxins in the body, radiation, and some medicines.

Iron deficiency, thalassemia, and sickle-cell anemia result from inadequate or improper

hemoglobin production.

The effector is the red blood cell with abnormally low hemoglobin in RBCs. The

response is decreased blood oxygen.

Iron deficiency anemia is caused by inadequate absorption or loss of iron. This is

probably the most common type of anemia, particularly in children.

Thalassemia anemia is a hereditarily determined inability to produce hemoglobin. There

are several forms of thalassemia that differ, depending on the number of defective genes

and form of inheritance. Symptoms of thalassemia can vary from mild to severe. Severe

forms can cause significant cardiovascular burden resulting in congestive heart failure.

The effector is the red blood cell. Abnormally formed hemoglobin in RBCs. The

response is decreased blood oxygen.

Sickle-cell anemia is a hereditarily determined inability to produce normal hemoglobin

molecules. The shape of the hemoglobin molecule distorts the erythrocyte into the

sickle-shaped cell that gives the disorder its name. These sickled cells rupture easily

thereby reducing blood carrying capacity. Furthermore, sickled cells tend to get stuck in

small blood vessels and further reduce blood supply.

Regardless of the cause and type of anemia, the condition usually results in the symptoms

of fatigue and intolerance to cold. Both of these symptoms are the result of decreased

cellular metabolism due to low oxygen levels in the body. This decreased cellular

metabolism provides less energy for muscle movement and heat generation.

Homeostasis of Heart Rate

The heart provides pressure to circulate blood so that all of the cells in the body receive

adequate oxygen and nutrients. Cardiac output is the amount of blood that is ejected

from the left ventricle of the heart each minute. Factors that determine cardiac output

include the heart rate (the number of beats per minute) and stroke volume (the volume of

blood ejected per beat).

These primary factors regulate stroke volume:

1. the degree of stretch of the heart in response to venous return prior to contraction,

2. the forcefulness of the contraction due to sympathetic stimulation; and

3. the pressure of the blood resisting ventricular ejection.

Heart rate is regulated primarily by sympathetic stimulation and adrenal medulla

hormones such as epinephrine and norepinephrine. The following explores the role of the

interplay between the sympathetic and parasympathetic outputs in regulating cardiac

output:

Under certain physiological conditions, cardiac output is inadequate to supply the oxygen

needed by the cells. Increased physical activity is an example for which elevated cardiac

output would be necessary.

Normal heart rate and stroke volume is a controlled condition with receptors in the

barareceptor, Proprioreceptor. The control center in the medulla oblongata increases

impulses and the output is increased sympathetic impulses. The effectors in the heart are

increased heart rate and increased contraction force. The response is increased cardiac

output, and increased contraction force results in greater stroke volume.

As long as the cells, especially skeletal muscle cells, require an increased cardiac output

to provide them with adequate oxygen, the heart rate and stroke volume will remain

elevated. However, once the muscles no longer need the greater level of oxygen, their

lower level of activity promotes greater parasympathetic stimulation. These increased

parasympathetic impulses inhibit heart rate and thereby reduce cardiac output.

Coronary heart disease (CAD) is a condition in which the coronary arteries are narrowed.

As a result, the heart muscle does not receive adequate blood or oxygen, and become

damaged. Throughout the industrialized world, heart disease is the number one cause of

premature death.

Two common forms of heart disease, myocardial infarction (heart attack) and congestive

heart failure (CHF) occur as a result of inadequate blood supply to the myocardium. In a

heart attack, heart muscle cells actually die and are replaced by scar tissue. CHF occurs

when the weakened heart muscle can no longer adequately pump blood.

Risk factors for heart disease are high cholesterol level, high blood pressure, smoking,

and obesity. These factors affect the controlled condition of inadequate cardiac output.

Receptors are baroreceptor, Proprioreceptor. The control center is the medulla oblongata.

The effector is decreased contraction force.

Congestive heart failure is an example of a positive feedback loop. As a result of the

damaged heart muscle, blood tends to pool in the atria which increases stretching of the

myocardium. At first, increased stretching elevates stroke volum

e, but eventually the heart muscle becomes overstretched and contracts less forcefully.

Less forceful contractions result in less blood flow through the coronary vessels which

further weakens the myocardium.

This cycle of the heart becoming an increasingly ineffective pump continues until the

heart can no longer move blood. At that point, blood pools in the lungs causing

pulmonary edema or in the extremeties causing peripheral edema.

Homeostasis of Blood Pressure

Providing adequate circulation of blood and the substances suspended and dissolved in it

is the major function of the cardiovascular system. Blood flows down a blood pressure

gradient produced during cardiac muscle contractions.

Normal blood pressure is a primary factor in moving blood. It is crucial to the normal

functioning of every organ in the body. Both the endocrine and the nervous systems

provide mechanisms of achieving blood pressure homeostasis. Hormonally controlled

mechanisms function more slowly than rapid nervous system mechanisms.

Blood pressure and flow are regulated by an autonomic reflex arc, one of the nervous

system mechanisms.

Blood loss is an example of a stimulus that would temporarily cause a drop in blood

pressure. Another example is beginning to exercise:

The controlled condition is decreased blood pressure. Receptors are baroreceptors in

aorta and carotid artery. The control center is the medulla oblongata whose output is

increased sympathetic nerve impulses, increased secretion of epinephrine and

norepinephrine. The effectors are:

Heart Vessels

Increased heart rate. Increased vasoconstriction.

Increased heart stroke volume.

Response Response

Increased cardiac output will Increased vascular resistance will

Elevate blood pressure. Elevate blood pressure.

The proper regulation of blood pressure guarantees the delivery of adequate oxygen and

nutrients to meet the metabolic needs of all of the body‟s cells. If blood pressure

becomes abnormally low (i.e. in the case of shock), then cellular metabolism becomes

dysfunctional and, if this condition persists, may result in death.

In industrialized nations, hypertension, or persistent elevated blood pressure, is one of the

most common disorders affecting the heart and blood vessels.

The cause of most cases of hypertension cannot be directly related to any one identifiable

factor. However, several risk factors including diet, stress, and an individual‟s genetic

makeup or heredity, predispose a person to hypertension.

Examples of stimuli that may result in hypertension are stress, genetic disposition, high

sodium diet, and obesity.

The controlled condition is excessive blood pressure. Receptors are baroreceptors in the

aorta and carotid artery. The control center is the medulla oblongata when output is

increased sympathetic nerve impulses, increased secretion of epinephrine and

norepinephrine.

The heart is the organ most commonly affected by hypertension. In an individual with

hypertension, the heart must work harder than normal to move the blood against the

elevated blood pressure to supply all of the organs with adequate levels of oxygen. This

overwork may result in inadequate perfusion of oxygen in the heart, potentially resulting

in cardiac ischemia (angina pectoris) or even cardial infarction (heart attack).

In the case of prolonged hypertension, brain arteries may burst causing a stroke and

eventual brain damage. In the kidneys, persistent high blood pressure thickens the

arterioles thereby reducing blood flow to the kidney cells and resulting in kidney damage.

The effectors are:

Heart Vessels

The response is:

Increased cardiac output Increased vasoconstriction

Hypertension is sometimes known as the “silent killer” because it adversely affects the

heart, kidney and brain before the person becomes aware of the damage.

Homeostasis of Blood Gas Levels

Maintaining proper levels of oxygen and carbon dioxide in the blood is crucial to

establishing each cell‟s normal metabolic processes. An important process occurs at the

alveoli of the lungs: oxygen is introduced into the blood and carbon dioxide is removed

from the blood.

The cells use oxygen to harvest chemical energy from fuel molecules. Carbon dioxide is

a byproduct of this process. Increasing carbon dioxide levels promotes the binding of

carbon dioxide with water to form carbonic acid which, in turn, then gives off a hydrogen

ion. Therefore, increased carbon dioxide levels lead to increased acidity (a lower pH

value) in the blood.

Blood levels of oxygen and carbon dioxide gases are regulated through an autonomic

reflex arc that alters respiration rate. An increase in respiration rate will increase oxygen

levels while decreasing carbon dioxide levels in the blood.

The regulation of blood gases is a vital process for maintaining normal health.

Inadequate oxygen (hypoxia) in the brain may result in fainting and the depression of the

control center in the medulla oblongata. If this process is not interrupted, it may trigger a

positive feedback loop causing even greater brain damage. Excessive changes in carbon

dioxide will alter blood pH and can potentially cause malfunction in many organs.

Respiratory failure is caused by the inability of the cardiovascular system to provide

adequate exchange of oxygen and carbon dioxide in the lungs. This condition occurs

when there is too little arterial oxygen or too much arterial carbon dioxide.

Chronic respiratory failure is characterized by respiratory acidosis, a condition in which

an individual‟s blood levels become acidic. Abnormally high CO2 would result in

respiratory acidosis.

Treatment for respiratory failure includes correcting initial cause (i.e. removing

pulmonary obstructions) and administering oxygen. Treatment of respiratory acidosis

may include intravenous administration of sodium bicarbonate to buffer and raise pH to

normal levels, bringing the body back to homeostasis.

Homeostasis of Gastric Secretions

The digestion and absorption of food plays an important role in maintaining normal

health. The stomach and intestines use the movements of smooth muscle as well as the

secretion of digestive juices, including acid, to break down food into smaller molecules

that can be absorbed into the blood. The absorbed food molecules will be used as energy

sources and to build other molecules needed for various cellular functions.

Smooth muscle movements are regulated by nervous system stretch reflexes. These

reflexes measure the increased amount of stretch in the stomach walls, resulting from

introduced food, and respond by stimulating greater stomach motility which aids

digestion.

The secretion of gastric juices, particularly hydrochloric acid, is regulated by a negative

feedback loop that monitors the level of acid secreted by the parietal cells of the stomach.

Ingested proteins act as buffers and tend to reduce the level of acidity in the stomach.

Ingested proteins and higher pH would result in increased nerve impulses from the gastric

chemoreceptors to the control center. This causes the parietal cells in the stomach to

increase HCl (hydrochloric acid) production. The response is increased gastric acidity.

This response increases gastric acid to promote digestion and returns pH to the normal

levels that were present before eating.

Excessive production of gastric acid (HCl), bacterial infection, and anti-inflammatory

drugs (NSAIDS) such as aspirin are the three main causes of Peptic Ulcer Disease

(PUD).

Peptic Ulcer Disease (PUD), a common digestive ailment, occurs in 5% - 10% of adults.

Peptic ulcers, crater-like lesions in the digestive mucosal membrane, occur where the

digestive tract is exposed to gastric acid.

When an individual has PUD, the protective functions of the digestive mucosa

(bicarbonate buffers from the pancreas, gastric mucus production, and epithelial tissue

regeneration) are overwhelmed and cannot function normally. As a result, the ulcerous

condition persists and cannot be repaired.

Stress, caffeine, alcohol, smoking, and NSAIDs are all stimuli that may result in

excessive production of gastric acid.

PUD is medically treated through the prescription of certain drugs, such as Pepcid TM

,

Zantac TM

, and Tagamet TM

, that slow the production of gastric acid by inhibiting

hydrogen ion pumps.

Homeostasis of Body Temperature

Maintaining a normal body temperature is a vital homeostatic process. The body

produces heat by expending chemical energy during normal cellular metabolism.

When the balance between the physiological factors that increase heat production and

those that contribute to heat loss is altered, changes in body temperature follow.

Thermoreceptors in the hypothalamus and skin monitor body temperature.

Impulses from the hypothalamus control outer trigger autonomic reflexes that act to alter

body temperature when it goes out of the normal range. Under abnormal body

temperatures, the hypothalamus also secretes thyroid-releasing hormone (TRH) which

promotes thyroid gland secretion.

Decreased temperature is a stimulus that will increase the frequency of nervous impulses

from the thermoreceptors to the control center.

Extremes in both high and low temperatures can be fatal. Body temperatures that are too

low can affect heart activity and cause rhythm aberrations. Next, we will explore the

homeostatic imbalances that occur when the body temperature rises above normal values:

When the body is unable to cool itself adequately, heat cramps, heat exhaustion, and heat

stroke can ensue.

Extreme increases in body temperature, like extreme changes in pH, can alter protein

structures. Changes in protein structures, especially enzymes, render them nonfunctional

and threatens the body‟s homeostasis.

The body‟s response to increasing body temperature is the opposite of its response to

decreasing body temperature. Decreased nerve impulses and less TRH is output from the

hypothalamus.

In addition to these heat-reducing mechanisms, cutaneous sweat glands are activated to

promote perspiration, an evaporative cooling mechanism.

These are two conditions that would result in a temperature imbalance.

Temperature imbalances occur following the loss of fluids and electrolytes causing multi-

organ disturbances to ensue. However, treatment for heat exhaustion and cramps is

simple. Replacing water and electrolytes and rest allows the patient to regain normal

homeostatic cooling ability.

Because normal cooling mechanisms do not work for victims of heat stroke, the patient

must be externally cooled by immersion in cool water to return the body to normal body

temperature values.

Homeostasis of Water and Ion Concentrations

Maintaining the body‟s water volume is crucial to normal cell and organ functions.

Inadequate blood volume, associated with decreased water volume, results in diminished

blood pressure. Low blood pressure reduces the flow of blood and therefore impacts the

distribution of blood components including cells, nutrients, and gases.

The amount of water in blood is affected by its osmotic pressure. Blood osmotic pressure

increases when greater concentrations of dissolved substances, particularly electrolytes,

and/or lesser amounts of water are found in the blood.

Under higher blood osmotic pressure levels, antidiuretic hormone (ADH) is released from

the posterior pituitary gland. The increased concentrations of ADH enhances water

reabsorption (retention) by the principal cells of the nephron of the kidney.

Maintaining the proper levels of ADH is instrumental in directly regulating blood

osmotic pressure. Furthermore, blood osmotic pressure indirectly affects blood volume,

blood pressure, and blood flow. As a result, blood osmotic pressure imbalances can have

adverse effects on multiple organs.

Diabetes insipidus (DI) is characterized by excessive dilute urine production. There are

two main forms of DI. Control DI is caused by inadequate production of ADH.

Nephrogenic DI, often the result of kidney damage or certain drugs, is caused by an

insensitivity of the principal cells in the nephron to ADH.

Medical treatment of diabetes insipidus involves taking a modified form of ADH which

returns the blood osmotic pressure to normal homeostatic values. Nephrogenic DI is

usually the result of damage to the kidney cell. When kidney cells are damaged, they do

not respond to ADH replacement therapy. In those cases, dialysis or kidney transplant

may be the only forms of treatment.

Homeostasis of Blood pH

Careful homeostatic regulation of the level of hydrogen ions (pH) in the blood is a critical

factor in the acid-base balance of body fluids. Some hydrogen ions enter the body as

good, but most hydrogen ions are produced as a result of cellular metabolism.

The body has three major ways to maintain pH: chemical buffers, urinary system

mechanisms and respiratory mechanisms. Chemical buffers, such as bicarbonate ions, act

quickly to prevent significant changes in hydrogen ion levels by binding with excess

hydrogen ions to remove them from solution. The urinary system acts slowly to remove

hydrogen ions by secreting the ions into urine which then leaves the body.

Increasing amounts of carbon dioxide cause the formation of more carbonic acid which,

in turn, will release H+ ions and thereby acidify the blood. Respiration rate is increased,

removing excess carbon dioxide.

Increased exercise is an example of a stimulus that would promote an increase in nerve

impulses from the chemoreceptors monitoring blood pH levels.

Maintaining the correct pH is critical because even small changes in hydrogen ion

concentrations may change the three-dimensional shape of body proteins. Any changes

in a protein‟s structure will adversely affect that protein‟s function. This is particularly

important to many enzymes that control cellular reactions in the body. Without

mechanisms to rid the body of excess hydrogen ions, death would soon result.

Normal blood pH values range from 7.35 to 7.45. When the blood pH is lower than 7.35,

a condition called acidosis occurs. When the blood pH is higher than 7.45, a condition

called alkalosis occurs. The body must compensate for these changes in blood pH in

order to maintain normal health.

If a pH imbalance caused by compromised respiratory function (respiratory acidosis or

alkalosis) occurs, then the urinary system must compensate for that imbalance. If the pH

is altered as a result of a metabolic problem (metabolic acidosis or alkalosis), then the

respiratory system must compensate to maintain normal pH values.

Damage to diaphragm or airways, lung disorder (i.e. emphysema) or depression of

respiratory center may result in respiratory acidosis.

Diarrhea (loss of bicarbonate ions), renal dysfunction or ketoacidosis (diabetes mellitus)

may result in metabolic alkalosis.

Treatments for acidosis, acidic pH imbalances, have to be rapid because very low pH

levels (below 7.0) can cause severe depression of the central nervous system which may

result in coma or death. Severe alkalosis, alkaline pH imbalances, tends to cause

overexcitability of the central nervous system which may result in muscle spasms,

convulsions and death.